Beyond Skin Deep: A Scientist’s Guide to IL-17, Neutrophils, and How to Treat Hidradenitis Suppurativa from Within

The IL-17 Signal: How New Research Unlocks the Secret to Treating Hidradenitis Suppurativa Naturally

My name is Jaap, and I am a biomedical scientist that also used to live with severe Hidradenitis Suppurativa, the kind that takes over your life. Today, I am completely asymptomatic because I learned how to heal Hidradenitis Suppurativa from within. More importantly, I’ve had the privilege of helping many other individuals with HS get their lives back too.

If you’re reading this, you know the feeling. It’s not just a skin issue. It’s a deep, relentless, and painful fire under the skin that seems to have a mind of its own. For decades, we’ve been told it’s a mysterious disease of the hair follicles, but we’ve always known it was something more, a whole-body problem. Now, groundbreaking research is finally catching up, and it’s shining a powerful light on the very engine of that fire. This new insight not only validates what many of us have felt but also helps us understand how to treat Hidradenitis Suppurativa on a much deeper level.

A recent study published in the British Journal of Dermatology took a deep dive into the molecular chaos happening inside HS lesions. And what they found confirms a crucial piece of the puzzle: two inflammatory signals, or cytokines, named Interleukin-17A (IL-17A) and Interleukin-17F (IL-17F), are acting like masterminds of the destruction.

Let’s break down what these scientists discovered and, more importantly, translate it into actionable wisdom for your healing journey. Because understanding the why behind the inflammation is the first step toward reclaiming your health.

The Real Culprits: A Storm of Neutrophils

Before we talk about the masterminds (IL-17), we have to talk about their soldiers: the neutrophils.

Think of your immune system like a highly trained army. Neutrophils are the frontline soldiers—the first responders. When you get a cut, they rush in to fight off bacteria. They are essential. But in HS, this system goes haywire. These soldiers are being called in for a war that doesn’t exist, and they start attacking your own body, creating the painful abscesses and tunnels we know all too well. This makes HS a neutrophilic dermatosis, a condition defined by an overwhelming infiltration of these destructive immune cells. The researchers showed this beautifully by staining HS tissue (Figure 1).

Figure 1 Legend: Visualizing the Inflammatory “Crime Scene” in HS Skin. Figure from Joseph Rastrick and colleagues.

• The Science: This figure compares healthy (nonlesional) skin to HS skin. In panel (a), the researchers used a stain for neutrophil elastase (in red), a destructive enzyme released by neutrophils. You can see a massive increase in these red-stained cells in the HS lesion (iii, iv) compared to the nonlesional skin (i, ii). In panel (b), they stained for the proteins IL-17A and IL-17F. Again, you see a dramatic increase in both of these inflammatory signals throughout the deep layers of the HS skin (iii, vi) compared to healthy skin and even psoriasis skin.
• What This Means for You: This is visual proof of the battle raging under your skin. The red stain in panel (a) is like finding the fingerprints of the immune cells (neutrophils) that cause the painful pus and tissue damage. Panel (b) shows us the generals (IL-17A and IL-17F) that are shouting the orders for these soldiers to attack. Unlike psoriasis, where the inflammation is more on the surface, in HS, this war is happening deep down in the dermis, which is why it’s so painful and destructive.

The Genetic “Shouting Match” Inside an HS Lesion

So, what’s calling all these neutrophils into our skin? The researchers looked at the genes being turned on or off in HS lesions compared to healthy skin. What they found was the genetic equivalent of a full-blown shouting match.

They identified over 5,000 dysregulated genes. And the ones shouting the loudest? Genes that scream, “SEND MORE NEUTROPHILS!” (Figure 2). These are genes with names like CXCL8, CSF3, IL1B, IL17A, and IL17F. They are all part of an intricate communication network that recruits, activates, and arms the neutrophil army. This isn’t just random inflammation; it’s a highly specific, coordinated attack orchestrated at the genetic level.

Figure 2 Legend: Mapping the Genetic Blueprint of HS Inflammation. Figure from Joseph Rastrick and colleagues.

• The Science: This is a “volcano plot” (a), a way to visualize changes in gene expression. Every dot is a gene. The dots in red are genes that are significantly “turned up” or upregulated in HS lesions. The researchers highlighted key genes involved in attracting neutrophils (like CXCL1, CXCL5, CXCL8) and the master signals themselves (IL17A, IL17F, IL1B). The charts on the right (b, c) confirm that the most significantly upregulated genetic signature in HS lesions belongs to neutrophils.
• What This Means for You: Think of your DNA as a massive library of instruction manuals. In HS lesions, the instruction manuals for inflammation and neutrophil attack are being photocopied and distributed thousands of times over. This plot proves that HS isn’t just a simple blockage; it’s a complex inflammatory disease with a distinct genetic footprint. It validates that the pain and swelling you feel are the result of a precise, powerful biological storm.

How to Treat HS: What Happens When You Block the Signals?

This is where the research gets really interesting and connects to modern medicine. The study analyzed skin samples from patients treated with a drug called bimekizumab, which blocks both IL-17A and IL-17F.

The results were clear: in patients who responded well to the drug, that genetic “shouting” for neutrophils quieted right down (Figure 3a). The signals were intercepted, the neutrophil soldiers weren’t recruited, and the skin began to heal.

More importantly, the researchers ran a lab experiment showing that blocking both IL-17A and IL-17F together was far more effective at stopping neutrophil migration than blocking either one alone (Figure 3c). This is a critical insight. It tells us that these two cytokines work together, and to truly calm the storm, you need to address both.

Figure 3 Legend: Intercepting the Attack Orders. Figure from Joseph Rastrick and colleagues.

• The Science: Panel (a) shows the expression levels of key neutrophil-attracting genes. You can see they are very high in baseline HS lesions (black) but are significantly reduced back toward normal levels (grey) in patients who responded to the IL-17A/F blocker (green). Panel (b) shows a heatmap of many HS-associated inflammatory genes in lab-grown skin cells, demonstrating that the dual blocker (Bimekizumab) was most effective at calming them down. Panel (c) is a neutrophil migration assay. It measures how many neutrophils move toward an inflammatory soup. Blocking IL-17A or IL-17F alone helped a bit, but blocking them both together (Bimekizumab) shut down the neutrophil migration by a whopping 44% more than blocking IL-17A alone.
• What This Means for You: This is powerful proof of concept. When you block the main signals driving the disease, the body can start to heal. This is the principle behind biologics. But it also reveals a crucial truth for our natural approach: to achieve remission, we need strategies that can quiet down this entire inflammatory network, not just one part of it. This is why a multi-layered, holistic strategy is so vital. We need to reduce the source of the fire that leads to IL-17 production in the first place.

The Knowledge Gap: Why HS Isn’t Psoriasis and the Role of IL-1ß

For a long time, scientists thought HS might be driven by the same pathway as psoriasis, another IL-17-driven disease. In psoriasis, a cytokine called IL-23 is the main trigger for IL-17 production. But drugs that block IL-23 have failed in HS clinical trials. Why?

This paper provides some incredible clues. They found that many of the IL-17-producing cells in HS lesions don’t even have the receptor for IL-23. It’s like trying to send a text message to a phone that’s turned off. The signal can’t get through.

So, what’s turning on IL-17 in HS? The study points a finger at another inflammatory molecule: IL-1ß. They found that IL-1ß can directly tell immune cells to pump out IL-17F, completely bypassing the normal IL-23 route. And guess what? HS lesions are flooded with IL-1ß (Figure 5). They also identified a special type of immune cell, called a MAIT cell, hanging around HS tunnels that is a potent producer of IL-17F (Figure 4).

Figure 4 Legend: Identifying a New “Cell of Interest” in HS. Figure from Joseph Rastrick and colleagues.

• The Science: Researchers used an advanced staining technique called RNAscope to find specific genetic messages inside cells. They found cells positive for TRAV1-2 and KLRB1 (panel a), which are markers for a unique immune cell called a MAIT cell. Crucially, they found that these MAIT cells (magenta dots) were also expressing the genetic message for IL-17F (black dots, panel b) and the receptor for the inflammatory signal IL-1 (black dots, panel c).
• What This Means for You: This introduces a new player in our HS story. MAIT cells are innate-like lymphocytes, part of a faster, more primal immune response. The fact that they are present, making the key inflammatory signal (IL-17F), and ready to respond to other signals (like IL-1) suggests they are important contributors to the chronic inflammation in HS tunnels.

Figure 5 Legend: The IL-1ß Connection—A “Backdoor” Pathway for Inflammation. Figure from Joseph Rastrick and colleagues.

• The Science: This figure shows data from lab experiments and human tissue. In panels (a) and (b), scientists stimulated human immune cells. Adding IL-1ß dramatically increased the production of IL-17F (green dots/bars) but had little effect on IL-17A (red dots/bars). In the tissue samples (panels c, d, e), they confirmed that cells making IL-1ß (magenta/black dots) are physically close to the cells making IL-17F (magenta dots) and that these IL-17F-producing cells have the receptor to “hear” the IL-1ß signal.
• What This Means for You: This is the missing link. This explains why HS is different from psoriasis and why targeting just one pathway often isn’t enough. It shows there’s a powerful backdoor for triggering inflammation in HS. The presence of IL-1ß can keep the IL-17F fire stoked. This is a critical piece of information because the root causes that we focus on in the HS Armor community, are known to have a profound impact on molecules like IL-1ß.

The HS Armor Philosophy: From Downstream Drugs to Upstream Solutions

And this brings us to the most important part of the discussion. This incredible research is a perfect example of the knowledge gap in conventional medicine.

Scientists are doing a phenomenal job of mapping the downstream effects, identifying the exact molecules like IL-17A and IL-17F that cause the damage. Drugs like bimekizumab are like highly sophisticated fire extinguishers, designed to put out the flames at the very end of the line. And for many, they can be a necessary and powerful shield.

But they don’t address the person holding the matches. They don’t ask: What is causing the flood of IL-1ß and other signals in the first place? Why is the immune system so primed to overreact?

This is where the HS Armor philosophy comes in. We at HS Armor focus on highly effective evidence-based nutrition and lifestyle change, and natural therapies and practices. Our goal is to address the upstream root causes. The entire premise of our approach is to reduce the systemic, body-wide inflammation that provides the fuel for the fire.

• Foundational Nutrition: An anti-inflammatory diet is designed to lower inflammatory signals like IL-1ß that originate from the gut and metabolic dysfunction.
• Strategic Lifestyle Changes: Managing stress and improving sleep directly impacts the immune system, making it less likely to launch these haywire attacks.
• Natural Therapies: Targeted, science-backed supplements can help modulate the immune response, making it more balanced and less trigger-happy.

This research doesn’t contradict our approach; it validates it on a molecular level. It gives us a beautiful roadmap of the chaos that ensues when the body is out of balance. The IL-17/neutrophil storm is the final, tragic act of a play that starts much, much earlier, with our diet, our environment, and our lifestyle.

Figure 6 Legend: The Full Story of an HS Lesion. Illustration from Joseph Rastrick and colleagues.

• The Science: This diagram synthesizes all the paper’s findings into a proposed model of how HS progresses. It starts with (a) follicular occlusion (a blocked hair follicle). This triggers an (b) early inflammatory lesion, where immune cells like macrophages and T cells are recruited, releasing IL-1ß, IL-17A, and IL-17F. This leads to a (c) progressed lesion with tunnel formation, where a vicious cycle is established. The IL-17 signals call in massive amounts of neutrophils, creating pus and breaking down tissue. This eventually leads to (d) advanced, interconnected tunnels.
• What This Means for You: This is the scientific story of what you feel in your body. It shows how a seemingly small event, a blocked follicle, can escalate into a devastating, chronic inflammatory process when the underlying immune system is out of balance. Our goal with a natural approach is to intervene at stage (b), to create a body environment where the immune system doesn’t overreact and escalate the situation, allowing the body to heal before the destructive cycle of stage (c) can ever take hold.

Key Takeaways

For those who like to skim, here are the crucial points:

• HS is a Neutrophil-Driven Disease: The pain and destruction in HS are primarily caused by an overabundance of immune cells called neutrophils.
• IL-17A & IL-17F Are the Masterminds: These two inflammatory signals are the key drivers telling the neutrophils to attack your skin. Blocking them both is more effective than blocking just one.
• HS Has a Unique Inflammatory Trigger: Unlike psoriasis, HS inflammation can be driven by IL-1ß, creating a backdoor pathway that keeps the fire burning.
• Science Validates a Root-Cause Approach: While drugs can block the downstream signals, true healing comes from addressing the upstream root causes (like diet and lifestyle) that trigger the inflammation in the first place.

Conclusion: Hope Through Understanding

This research is more than just data; it’s a message of hope. It tells us that HS is not a random, mysterious curse. It’s a logical (though destructive) process that we are beginning to understand with incredible clarity. And with that understanding comes power.

The path to treating HS naturally isn’t about ignoring this science; it’s about embracing it. It’s about using this knowledge to make smarter, more strategic choices. It’s about building your own HS Armor, layer by layer, to create a body where this inflammatory cascade simply doesn’t have the fuel to start. Seeing how these foundational changes have helped so many HS patients truly brings this research to life. Healing is possible, and science is helping to light the way.

References

1. Rastrick, J., Edwards, H., Ferecskó, A. S., Le Friec, G., Manghera, A., Page, M., & Shaw, S. (2025). The roles of interleukin (IL)-17A and IL-17F in hidradenitis suppurativa pathogenesis: evidence from human in vitro preclinical experiments and clinical samples. British Journal of Dermatology, 192(4), 660–671. https://doi.org/10.1093/bjd/ljae442

Important Medical Disclaimer

1. Not Medical Advice: All content and information on this website is for informational and educational purposes only. It does not constitute medical advice and is not a substitute for professional diagnosis, treatment, or consultation with a qualified healthcare provider.

2. My Role and Qualifications: I am a biomedical scientist and PhD candidate and share information from that perspective, combined with my personal experience as a patient with Hidradenitis Suppurativa. However, I am not a medical doctor, physician, or registered healthcare professional. Do not consider our relationship a doctor-patient relationship.

3. Consult Your Doctor: Always seek the advice of your medical doctor or another qualified health professional with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay seeking it because of something you have read on this website. If you suspect you are experiencing a medical emergency, or a severe infection, do not rely on this website or the HS Armor community, please call your local emergency services or go to the nearest emergency room immediately.

4. A Critical Warning on Medication: Pharmaceutical drugs are a crucial tool in managing Hidradenitis Suppurativa for many people. Under absolutely no circumstances should you ever alter, reduce, or stop taking your prescribed medication without the explicit direction of the doctor who prescribed it. Doing so can be dangerous. Always consult with your doctor before doing anything related to your treatment plan.

5. No Liability: Your use of this website and reliance on any information provided is solely at your own risk.

6. Individual Results May Vary: Every patient’s biological baseline, genetics, and adherence to the protocol is different. Therefore, I cannot guarantee specific results, cures, or timelines for your Hidradenitis Suppurativa.

7. Scientific and Expressive Freedom: The articles published on this blog are distinct from formal peer-reviewed academic literature. They serve as an independent platform for my personal viewpoints, scientific hypotheses, and philosophical reflections as an independent scientist and HS patient. While grounded in biomedical research, I exercise a degree of expressive freedom to translate rigid academic data into insights from a patient perspective. These writings are my personal meditations on the science of HS and should be read as my individual perspective, not as universally accepted clinical consensus or formal peer-reviewed literature.